Elimination of Porphyromonas gingivalis inhibits liver fibro
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Non-alcoholic steatohepatitis (NASH) is a critical liver disease showing potential progression to liver cirrhosis/cancer. Previously, researchers have reported that odontogenic infection of Porphyromonas gingivalis (P.g.), a major periodontal pathogen, exacerbates fibrosis in NASH through fibrosis mediators such as Transforming growth factor-β1 (TGF-β1) and Galectin-3 productions.

In this study, investigators determined the effects of therapeutic interventions using antibiotics on NASH progression induced by P.g.-odontogenic infection.

To eliminate P.g. infection, a macrolide antibiotic (Azithromycin: AZM) was applied locally and/or systemically to high fat diet-induced NASH mouse model with P.g.-odontogenic infection. After AZM-treatment, liver and periodontal tissues have been analyzed with focusing on inflammation markers such as TNF-α and IL-1β, and fibrosis markers such as Galectin-3, phosphorylated Smad2 (pSmad2; key signaling molecule of TGF-β1), number of hepatic crown-like structures (hCLS). Further, the Non-alcoholic fatty liver disease Activity Score (NAS), a common histological scoring system, and fibrosis area were evaluated.

P.g.-odontogenic infection significantly increased the expression of Tnf-α, Il-1β, Galectin-3, and pSmad2, the number of hCLS and NAS score whereas elimination of P.g.-odontogenic infection, especially local with/without systemic application, significantly inhibited them.

This study suggests that elimination of P.g.-odontogenic infection inhibited NASH progression induced by P.g.-odontogenic infection.

Journal of Clinical Periodontology
Source: https://doi.org/10.1111/jcpe.13523
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